AUTHOR AND EDITOR INFORMATION

Section 1 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

INTRODUCTION

Section 2 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Background

Meningitis is an infection of the linings of the brain and ventricles that can be divided into 3 general categories: pyogenic, granulomatous, and lymphocytic. Pyogenic (bacterial) meningitis is a potentially life-threatening disease that consists of inflammation of the meninges and the underlying subarachnoid cerebrospinal fluid (CSF). The specific infective agents that are involved vary among different patient age groups, and the inflammation may evolve into ventriculitis, empyema, cerebritis, and abscess formation. If not treated, bacterial meningitis may lead to lifelong debility or death.

For excellent patient education resources, visit eMedicine's Brain and Nervous System Center. Also, see eMedicine's patient education articles Meningitis in Adults, Meningitis in Children, and Brain Infection.

Pathophysiology

Usually, the brain is naturally protected from the body's immune system by a barrier the meninges create between the bloodstream and the brain. Normally, this protection is an advantage because the barrier prevents the body from attacking itself. However, in meningitis, the barrier can become a problem; once bacteria or other organisms have found their way to the brain, they are somewhat isolated from the immune system and can spread. When the body tries to fight the infection, the problem can worsen; blood vessels become leaky and allow fluid, white blood cells, and other infection-fighting particles to enter the meninges and brain. This process, in turn, causes brain swelling and can eventually result in decreasing blood flow to parts of the brain, worsening the symptoms of infection.

Pyogenic organisms may reach the leptomeninges and cause meningitis via several routes, including the following:

• Bacterial seeding usually occurs via hematogenous spread. Organisms usually enter the meninges through the bloodstream from other parts of the body. Many meningitis-causing bacteria are carried in the nose and throat, often without symptoms in the carrier.  

• Bacterial seeding results in increased permeability of the blood-brain barrier, cerebral edema, and the presence of toxic mediators in the CSF. Inflammations are characterized by polymorphonuclear cell infiltration and extensive fibrinous exudation, which extends throughout the CSF, basal cisterns, and cranial nerves. Acute leptomeningitis results in congestion and hyperemia of the pia-arachnoid and distention of the subarachnoid space by the exudates. 

• Local extension from contiguous extracerebral infection (eg, otitis media, mastoiditis, or sinusitis) is a common cause. Possible pathways for the migration of pathogens from the middle ear to the meninges include the following:
  
  
  • A systemic route in the bloodstream
  • Along preformed tissue planes (eg, posterior fossa)
  • Temporal bone fractures
  • The oval or round window membranes of the labyrinths

Congenital malformation of the stapedial footplate has also been implicated.  

• Direct implantation of bacteria into the meninges occurs less frequently and is a complication of head and neck surgery, penetrating head injury, comminuted skull fracture, and osteomyelitic erosion. Skull fractures can tear the dura and cause a CSF fistula, especially in the region of the frontal ethmoid sinuses. Patients with any of these conditions are at risk for bacterial meningitis.

• The pathogenesis of neonatal meningitis is related to labor delivery as a result of colonized pathogens in the maternal intestinal or genital tract, immaturity, and environment.

In 50% of patients, several complications may develop in the days to weeks following infection.

• Infarction and venous thrombosis: In cerebral infarction, endothelial cells swell, proliferate, and crowd into the lumen of the blood vessel, and inflammatory cells infiltrate the blood vessel wall. Foci of necrosis develop in the arterial and venous walls and induce arterial and venous thrombosis. Venous thrombosis is more frequent than arterial thrombosis, but both arterial and venous cerebral infarctions can be seen in 30% of patients.

• Cerebritis and abscess: Inflammation often extends along the perivascular (Virchow-Robin) spaces into the underlying brain parenchyma. Commonly, cerebritis results from direct spread of infection, either from otorhinologic infection or meningitis (including retrograde septic thrombophlebitis) or from hematogenous spread from an extracranial focus of infection. Parenchymal involvement, with edema and mass effect, may be localized or diffuse. Cerebritis can evolve to frank abscess formation in the gray matter–white matter junction.

• Subdural effusions and empyema: In children with meningitis who are younger than age 1 year, 20-50% of cases are complicated by sterile subdural effusions. Most cases are transient and small to moderate in size. Of these effusions, 2% are infected secondarily and become subdural empyemas. In the empyema, infection and necrosis of the arachnoid membrane permits formation of a subdural collection.  

• Ventriculitis: Ventriculitis may occur through the involvement of the ependymal lining of the ventricles in 30% of patients. This complication is especially common in neonates, with an incidence as high as 92%. The organisms enter the ventricles via the choroid plexuses. As a result of reduced CSF flow, and possibly reduced secretion of CSF by the choroid plexus, the infective organisms remain in the ventricles and multiply.

• Hydrocephalus: Ventriculomegaly can occur early or late in the course of meningitis and is usually transient and mild to moderate in severity. As a result of the subarachnoid inflammatory exudate, CSF pathways may become obstructed, leading to hydrocephalus. Exudates in the foramina of Luschka and Magendie can cause noncommunicating hydrocephalus, whereas exudates that accumulate in the basilar cisterns or over the cerebral convexity can develop into communicating hydrocephalus.

• Cerebral edema: Some degree of cerebral edema is common with bacterial meningitis. This complication is an important cause of death.

• Seizures: Seizures are a common and important complication that occur in approximately one fifth of patients. The incidence is higher in patients younger than age 1 year, reaching 40%. Approximately one half of patients with this complication have repeated seizures. Patients die as a result of diffuse CNS ischemic injury or from systemic complications.

Anyone can contract bacterial meningitis, but the disease occurs most commonly in infants and children. Meningitis is caused by various pathogens depending on the patient’s age group.¹ In neonates, Group B (49%) and non-group B Streptococcus species, Escherichia coli (18%), and Listeria monocytogenes (7%) are the most common causative organisms.¹ Children and infants acquire meningitis from infection with Haemophilus influenzae (40-60%), Neisseria meningitidis (25-40%), and Streptococcus pneumoniae (10-20%). The sources of adult meningitis include S pneumoniae (30-50%), N meningitidis (10-35%), Staphylococcus (5-15%), other Streptococcus species, H influenzae (1-3%), gram-negative bacilli (1-10%), and L monocytogenes.

Risk factors for bacterial meningitis include pulmonary infection, otitis media, mastoiditis, head trauma, alcoholism, splenectomy, sickle cell disease, and immunosuppression. People who have had close or prolonged contact with a patient with meningitis caused by N meningitidis or H influenzae can also be at increased risk. This includes people in the same household or daycare center or anyone who has direct contact with the oral or nasal discharges of a patient with bacterial meningitis.

Frequency

United States

With almost 8000 cases and 2000 deaths occurring annually, bacterial meningitis continues to be a significant source of morbidity and mortality.

• The incidence of neonatal bacterial meningitis is 0.25-1 case per 1000 live births. In addition, the incidence is 0.15 case per 1000 full-term births and 2.5 cases per 1000 premature births. Approximately 30% of newborns with clinical sepsis have associated bacterial meningitis.
• The frequency of H influenzae type b disease has been markedly reduced, but N meningitidis causes approximately 4 cases per 100,000 children aged 1-23 months. The risk of secondary meningitis is 1% for family contacts and 0.1% for daycare contacts. The rate of meningitis caused by S pneumoniae is 6.5 cases per 100,000 children aged 1-23 months.
• Statistics show an increased incidence in persons aged 60 years and older, independent of other factors. Annual incidences are 1.7-7.2 cases per 100,000 adults, and the mean annual incidence has been reported as 3.8 cases per 100,000 adults. Of patients with bacterial meningitis, 61% had no previous or present accompanying diseases that may have predisposed them to meningitis.

International

In parts of Africa, widespread epidemics of meningococcal meningitis occur regularly. In 1996, the biggest wave of meningococcal meningitis outbreaks ever recorded was in West Africa. An estimated 250,000 cases and 25,000 deaths occurred in Niger, Nigeria, Burkina Faso, Chad, and Mali.

Mortality/Morbidity

Bacterial meningitis can be extremely serious. Morbidity, mortality, and prognosis depend on the pathogen, the patient's age and condition, and the severity of acute illness.

• Mortality rates are highest in the first year of life, decrease in mid life, and increase again in old age. Bacterial meningitis is fatal in 1 in 10 cases, and 1 in 7 survivors is left with a severe handicap, such as deafness or brain injury. Among bacterial pathogens, pneumococcal meningitis causes the highest mortality rate, which is 20-30% in adults and 10% in children, with a morbidity rate greater than 30% in those who are affected. Patients with meningococcal meningitis have a better prognosis, with a mortality rate of 4-5%; however, patients with meningococcemia have a poor prognosis, with a mortality rate of 20-30%.
• The prognosis depends on both the severity and the cause of the meningitis. Despite effective antimicrobial and supportive therapy, mortality rates among neonates remain high, with significant long-term sequelae in survivors. Bacterial meningitis also causes long-term sequelae and results in significant mortality beyond the neonatal period. Prolonged or difficult-to-control seizures are predictors of a complication. Cerebral infarction and edema are predictors of poor outcome, as are the signs of disseminated intravascular coagulopathy and endotoxic shock.
• Advanced bacterial meningitis can lead to brain damage, coma, and death. Long-term sequelae are seen in as many as 30% of survivors and vary with etiologic agent, patient age, presenting features, and hospital course. Patients usually have subtle CNS changes. Serious complications include hearing loss, cortical blindness, other cranial nerve dysfunction, paralysis, muscular hypertonia, ataxia, multiple seizures, mental motor retardation, focal paralysis, ataxia, subdural effusions, hydrocephalus, and cerebral atrophy.

Race

Statistically, blacks appear to contract meningitis more frequently than do people of other races.

Sex

In neonates, the male-to-female ratio is 3:1. Male infants have a higher incidence of gram-negative neonatal meningitis. In adults, group B Streptococcus infection affects men and women equally.

Age

Nonepidemic meningitis is most common in neonates, infants, and children. Epidemic meningitis can occur at any age. The average age for those affected with bacterial meningitis is 25 years.

• Most patients are children younger than age 5 years, and 70% of cases occur in children younger than age 2 years.
• Rates of bacterial meningitis are highest among infants. The peak incidence is at age 3-8 months.

Anatomy

Infections of the CNS can be divided into 2 broad categories: those primarily involving the meninges (meningitis) and those primarily confined to the parenchyma (encephalitis).

The meninges are membranes that enclose the brain and spinal cord. The membrane is found in 3 layers: the dura (a tough outer layer), the arachnoid (a lacy weblike middle layer), and the subarachnoid space (a delicate, fibrous inner layer that contains many of the blood vessels that feed the brain and spinal cord).

Meningitis is anatomically divided into inflammation of the dura, sometimes referred to as pachymeningitis, which is less common, and leptomeningitis, which is more common and is defined as inflammation of the arachnoid tissue and subarachnoid space.

On the basis of the finding of abundant pus, pachymeningitis most often results from a bacterial infection (usually due to staphylococcal or streptococcal organisms) that is localized to the dura. The source of the organisms is most often a skull defect (eg, skull fracture), an infection of the paranasal sinuses, or cranial osteomyelitis. Leptomeningitis is the type of meningitis usually referred to when the term meningitis is used alone.

The most common cause of meningeal inflammation is irritation caused by bacterial or viral infections. The organisms usually enter the meninges through the bloodstream from other parts of the body. Most cases of bacterial meningitis are localized over the dorsum of the brain; however, under certain conditions, meningitis may be concentrated at the base of the brain, such as with fungal diseases and tuberculosis (TB).

Depending on the severity of bacterial meningitis, the inflammatory process may remain confined to the subarachnoid space. In less severe forms, the pial barrier is not penetrated, and the underlying parenchyma remains intact. However, in more severe forms of bacterial meningitis, the pial barrier is broken, and the underlying parenchyma is invaded by the inflammatory process. Thus, bacterial meningitis may lead to widespread cortical destruction, particularly when left untreated.

Clinical Details

Meningitis usually develops rapidly. The clinical presentation varies with the age of the patient, and there is a distinct difference between the signs and symptoms in neonates and young infants and those in older children and adults.

Symptoms

High temperature, headache, and a stiff neck are common symptoms of meningitis in anyone older than age 2 years. These symptoms can develop over several hours or over 1-2 days. Other symptoms may include nausea, vomiting, discomfort when the patient looks into bright lights, confusion, and sleepiness. Occasionally, if the patient has been taking antibiotics for another infection, the symptoms can take longer to develop or they may be less intense.

About 85% of adults and children exhibit the classic triad (fever, headache, neck stiffness) of bacterial meningitis.¹ One quarter of affected patients have a fulminant onset within 24 hours of infection, and there may be a history of a respiratory illness within the preceding 7 days (50%). Other presenting symptoms include vomiting in 35% and impaired consciousness.

Newborns and small infants may not present with the classic symptoms, or the symptoms may be difficult to detect. The infant may only appear to be slow or inactive, or he or she may be irritable, vomiting, or feeding poorly. Other symptoms in this age group include temperature instability, high-pitched crying, respiratory distress, and/or bulging fontanelles (late sign in one third of neonates).

As bacterial meningitis progresses, patients of any age may have seizures (30% of adults and children; 40% of newborns and infants).

Signs

Approximately half of affected adults show signs of meningeal irritation such as nuchal and/or spinal rigidity and a positive Kernig and/or Brudzinski sign.¹ On physical examination, a skin rash caused by meningococcal meningitis (50%), H influenzae, pneumococcal meningitis, echovirus type 9, or Staphylococcus aureus may be present.¹ Other neurologic signs include cranial nerve palsies, focal cerebral signs (10-20%), and papilledema (<1%).

Early diagnosis and treatment of bacterial meningitis are essential. Usually, the diagnosis is made by laboratory examination of cultured bacteria from a CSF sample. More specialized laboratory tests, which may include other cultures of CSF and blood specimens, are needed for identification of the bacteria and the serogroup, as well as the organism’s susceptibility to antibiotics. However, starting treatment early in the course of the disease is crucial. Appropriate antibiotic treatment for the most common types of bacterial meningitis should reduce the risk of death to less than 15%, although the risk is higher among elderly patients.

Preferred Examination

Acute bacterial meningitis is a clinical diagnosis that is established by the affected patient's history, physical examination findings, and laboratory results.

Neuroimaging studies are typically used to monitor complications such as hydrocephalus, subdural effusion, empyema (see Images 1-5, 8-10), and infarction (see Images 8-9, 11) to exclude parenchymal abscess (see Images 4, 7, 12) and ventriculitis. Neuroimaging is indicated in patients who have evidence of head trauma, sinus or mastoid infection (see Images 1-4), skull fracture, and congenital anomalies.

Imaging studies performed in patients with acute meningitis may provide normal findings. The results of an imaging study do not exclude or prove the presence of acute meningitis; prompt diagnosis depends on an accurate clinical assessment. Lumbar puncture is the single most important diagnostic study.

Computed tomography (CT) scanning is often performed first to exclude contraindications for lumbar puncture. Nonenhanced CT scans and magnetic resonance images (MRIs) of patients with uncomplicated acute bacterial meningitis may be unremarkable (Image 13).

Currently, MRI is the most sensitive imaging modality because the presence and extent of inflammatory changes in the meninges, as well as complications, can be detected. MRI is superior to CT scanning in the evaluation of patients with suspected meningitis, as well as in demonstrating leptomeningeal enhancement and distention of the subarachnoid space with widening of the interhemispheric fissure, which is reported to be an early finding in severe meningitis.

Effusion, hydrocephalus, cerebritis, and abscess can be evaluated well with CT scanning and ultrasonography (US) in infants; however, MRI is the most effective modality for localizing the level of the pathology.

Chest radiographs may be obtained to look for signs of pneumonia or fluid in the lungs, especially in children.

Limitations of Techniques

In uncomplicated cases of purulent meningitis, early CT scans and MRIs usually demonstrate normal findings or small ventricles and effacement of sulci (see Images 13-15). The value of CT scanning in the early diagnosis of subdural empyema is limited because of the presence of bone artifact.

Enhancement of the meninges is seen on contrast-enhanced CT scans and MRIs in cases of bacterial meningitis (see Images 2, 6, 15-17). However, meningeal enhancement is nonspecific and may also be caused by the following 5 different etiologic subgroups²:

• Infectious
• Carcinomatous meningitis
• Reactive (eg, surgery, shunt, trauma)
• Chemical (eg, ruptured dermoid and cysticercoid cysts, intrathecal chemotherapy)
• Inflammatory (eg, sarcoidosis, collagen vascular disease)

DIFFERENTIALS

Section 3 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Other Problems to Be Considered

Meningeal reaction (surgery, shunt, trauma)
Fungal meningitis
Chemical meningeal reaction (ruptured dermoid and cysticercoid cysts, intrathecal chemotherapy)
Sarcoidosis
Collagen vascular disease
HIV encephalitis

RADIOGRAPH

Section 4 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Findings

Plain radiographs do not have diagnostic importance in bacterial meningitis.

Chest radiography may be obtained to look for signs of pneumonia or fluid in the lungs. As many as 50% of patients with pneumococcal meningitis also have evidence of pneumonia on initial chest images.

CT SCAN

Section 5 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Findings

The most important role of CT scanning in imaging patients with meningitis is to identify contraindications of a lumbar puncture and complications that require prompt neurosurgical intervention; such complications include symptomatic hydrocephalus, subdural empyema, and cerebral abscess.

• Nonenhanced CT scan findings may be normal (>50% of patients),  or the studies may demonstrate mild ventricular dilatation and effacement of sulci (see Image 13), cerebral edema (see Image 11), and focal low-attenuating lesions (see Image 10).
• Obliteration of the basal cisterns may result from increased attenuation, perhaps owing to the presence of exudate in the subarachnoid space or leptomeningeal hyperemia. Increased attenuation in the CSF spaces due to meningitis may simulate acute subarachnoid hemorrhage on CT scans.
• CT scans for patients with suggested meningitis must be performed with iodinated contrast material. Diffuse enhancement of the subarachnoid space is characteristic (see Image 6).
• Curvilinear meningeal enhancement over convexities, interhemispheric and sylvian fissures, and obliteration of basal cisterns are usually seen on contrast-enhanced CT scans. Dural enhancement also may occur.
• Contrast-enhanced CT scans help in detecting complications of meningitis, such as subdural effusion/empyema (see Images 1, 5, 8-10), venous thrombosis, infarction (see Images 8-9, 11), cerebritis/abscess (see Images 6-7, 12), hydrocephalus, and ventriculitis.
  
  
  • Subdural empyema/effusion: Subdural effusion is a common complication of meningitis, especially in young children. CT scans have shown that as many as 25-40% of children develop this complication during or after treatment for meningitis.  Some subdural effusions resolve spontaneously, whereas others may require aspiration or drainage. Important diagnostic features on CT scans are high-attenuating effusions from the CSF and prominent enhancement of the margin of an empyema (see Images 5, 8, 10, 19). The marked degree of enhancement of an empyema that is seen on CT scan rarely occurs in cases of a subdural hematoma, although a thin rim of enhancement is not uncommon in imaging of a chronic subdural hematoma.
  • Venous thrombosis: Sinus thrombosis can be demonstrated on CT scans. In the acute phase (when the clot is dense), a hyperattenuating thrombus can be seen in the sagittal sinus on a nonenhanced scan. The so-called empty delta sign, which is a triangle of decreased attenuation in the posterior portion of the affected sinus, can be seen on contrast-enhanced CT scans and is visible only after the clot becomes less dense than the contrast-enhanced blood that flows around it.
  • Infarcts: CT scanning is reliable for the diagnosis of infarcts, which tend to be sharply marginated and confined to a specific arterial vascular territory (see Image 8). Commonly, multiple lacunar infarcts are seen in the distribution of perforating vessels in the brainstem, basal ganglia, and white matter (see Images 9, 11).
  • Cerebritis and abscess: In cerebritis, CT scans can show ill-defined areas of low attenuation, which are evidence of edema in the affected brain (see Image 6). On nonenhanced CT scans, abscesses, which are most commonly located near the gray matter–white matter junction, can appear as areas of low attenuation with a thin wall of slightly increased attenuation. After the administration of contrast material, the abscess wall and surrounding inflammatory tissue enhancement are ring shaped (see Images 5, 7, 12).
  • Ventriculitis: A complication of bacterial meningitis, ventriculitis is seen commonly in neonatal meningitis; ependymal enhancement can be seen on contrast-enhanced CT scans.
  • Hydrocephalus: Obstructive hydrocephalus can occur with chronic inflammatory changes in the subarachnoid space or in cases of ventricular obstruction. CT scans can demonstrate hydrocephalus.

Sequelae from meningitis may be depicted on CT scans as periventricular and meningeal calcifications, localized areas of encephalomalacia, porencephaly, and ventricular dilatation secondary to brain atrophy.

Degree of Confidence

The value of CT scanning in the early diagnosis of subdural empyema and effusion has been controversial as this modality may not detect meningitis, especially nonenhanced CT scans in the early stage (see Image 13). Normal results on CT imaging do not exclude the presence of acute meningitis.

False Positives/Negatives

Meningeal enhancement is nonspecific and may be caused not only by bacterial meningitis, but also by neoplasm, hemorrhage, sarcoidosis, and other noninfectious inflammatory disorders.

MRI

Section 6 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Findings

Routine contrast-enhanced brain MRI is the most sensitive modality for the diagnosis of bacterial meningitis because it helps to detect the presence and extent of inflammatory changes in the meninges as well as complications. The increased sensitivity and specificity of MRI results from direct multiplanar imaging, increased contrast resolution, and the absence of artifact caused by bone.

Some authors suggest performing MRI with a high dose of contrast material (0.3 mmol/kg), which is the most important factor.³ They also recommend imaging immediately after the injection and then performing magnetization transfer imaging, which can help to depict abnormal meningeal enhancement and which facilitates the diagnosis of early brain meningitis.³

• Nonenhanced MRIs of patients with uncomplicated acute bacterial meningitis may demonstrate obliterated cisterns and the distention of the subarachnoid space with widening of the interhemispheric fissure, which is reported to be an early finding in severe meningitis or may be unremarkable.
  
  
  • T2-weighted images are sensitive to abnormal tissue water distribution and, thus, may show cortical hyperintensities that are reversible and believed to represent edema (see Images 3, 14, 18).
  • Diffuse enhancement of the subarachnoid space is characteristic.
• Contrast-enhanced MRI has been shown to be more sensitive than CT scanning in the detection of meningeal inflammation.
  
  
  • Gadolinium-enhanced MRI studies can demonstrate abnormal leptomeningeal enhancement that more closely approximates the extent of inflammatory cell infiltration (see Images 2, 15, 17).
  • Extension of enhancing subarachnoid exudate deep into the sulci can be seen in severe cases (see Image 17).
  • Dural enhancement may occur (see Images 16-17).
• Revealing the cause of meningeal infection is best accomplished with MRI. MRI can help to detect inflammatory changes in the paranasal sinuses and mastoid air cells, which are usually depicted as areas of increased signal intensity on T2-weighted images (see Images 3-4). Enhancement may be prominent (see Image 2).
• MRI also can help to exclude congenital and posttraumatic calvarial defects.
• Coronal and sagittal thin-section, heavily T2-weighted MRIs may show CSF leaks, which may be the source of infection in cases of recurrent meningitis.
• Plain and contrast-enhanced MRIs help to depict the complications of meningitis better than other images. Such complications include empyema/effusion, cerebritis/abscess (see Images 4, 17-18), venous thrombosis, venous and arterial infarcts, ventriculitis, hydrocephalus, and edema (with or without cerebral herniation).
  
  
  • Subdural empyema/effusion
    
    
    • Sterile fluid collections may develop within the subdural space in patients with meningitis. Effusions may be slightly hyperintense relative to CSF on MRIs and are most commonly located in cerebral convexities and interhemispheric fissures (see Images 2-4).
    • Occasionally, a portion of the medial subjacent cerebral surface of an effusion demonstrates mild enhancement, presumably from an inflammatory surrounding membrane. These effusions are not empyemas and typically resolve spontaneously.
    • In the early stages of subdural empyema, T2-weighted images can demonstrate a thin hyperintense convexity and interhemispheric collection usually not visible on CT scans (see Images 3-4).
    • Paratentorial and subtemporal extension is well demonstrated on coronal MRIs.
    • Prominent enhancement of the margin of an empyema is an important diagnostic feature on MRI and results from the formation of a membrane of granulomatous tissue on the leptomeninges and from inflammation in the subjacent cerebral cortex (see Image 2).
    • On MRI, even a noninfected subdural hematoma enhances markedly on gadolinium-enhanced images.
    • Subdural empyema may be differentiated from subacute/chronic subdural hematoma. A hematoma is hyperintense on T1- and T2-weighted images because of the presence of extracellular methemoglobin and other forms of iron.
  • Cerebritis/abscesses: Cerebritis is the earliest stage of a purulent brain infection. If bacterial cerebritis is not successfully treated medically, the affected portion of the brain liquefies and a surrounding capsule of granulation tissue and collagen forms, resulting in abscess formation. The corticomedullary (gray matter–white matter) junction is the most commonly affected location, and the frontal and parietal lobes are the most frequent sites. Less than 15% of intracranial abscesses occur in the posterior fossa. Multiple abscesses are uncommon except in patients who are immunocompromised. MRI findings of pyogenic brain abscesses are characteristic.
    • On MRIs, stage I cerebritis appears as an ill-defined edematous area on both T1- and T2-weighted images (see Images 17-18).
    • In late stage II cerebritis/early abscess, the abscess wall is hyperintense on T1-weighted images and slightly hypointense on T2-weighted images.
    • In stage III (subacute abscess), the abscess wall is hyperintense on both T1- and T2-weighted images.
    • In stage IV (chronic phase), the abscess wall is isointense on T1-weighted MRIs and markedly hypointense on T2-weighted MRIs.
    • Although abscesses in stages II-IV all exhibit ring-type enhancement after the infusion of a paramagnetic contrast agent, better edge definition is seen in the enhancing wall of stage II lesions than in stages III and IV.
    • Abscesses may imitate brain tumors and can be differentiated with use of proton magnetic resonance spectroscopy. Brain tumors usually demonstrate elevated choline and possibly decreased creatine peaks, as well as N-acetyl-aspartate peaks. Abscesses do not demonstrate these abnormal peaks; instead, they have lactate peaks and the lipid peaks of amino acids.
  • Venous thrombosis: Thrombosis of the deep veins, cortical veins, and venous sinuses is an uncommon complication of meningitis; however, thrombosis more often develops in the presence of superimposed dehydration.
    
    
    • Gradient-echo and spin-echo MRIs can demonstrate cortical vein and/or dural sinus thrombosis, as well as the characteristic signal-intensity properties of acute and subacute hemorrhagic infarctions.
    • MRI-aided diagnosis for acute and chronic sinus thrombosis may be complex; however, sinus thrombosis is readily diagnosed when the thrombus is subacute because they are hyperintense on T1-weighted images.
    • Magnetic resonance venography (2-dimensional time-of-flight or phase-contrast) can aid the diagnosis of venous sinus thrombosis.
    • Cavernous sinus thrombosis is an uncommon sequela of meningitis. The signal intensity of this condition varies depending on the state of infection, inflammation, and clot evolution. The sinus may be enlarged with a narrowed or occluded cavernous carotid artery. T2-signal prolongation may occur in the adjacent clivus or petrous apex.
  • Venous and arterial infarcts: Venous infarcts are diagnosed on the basis of their characteristic location and appearance.
    
    
    • Typically, infarcts from a sagittal sinus thrombosis involve the parietal lobes; those from the straight sinus/vein of Galen thrombosis involve the thalami; and infarcts from the transverse sinus or sigmoid sinus thrombosis involve the temporal lobe.
    • Arterial infarctions in bacterial meningitis are usually the result of arteritis caused by involvement of the vascular spaces and the arterial walls. When major cerebral arteries are involved, large cortical infarctions result. Frequently, multiple lacunar infarcts are seen in the distribution of the perforating vessels in the brainstem, basal ganglia, and white matter.
  • Ventriculitis: The infecting organisms enter the ventricles via the choroid plexuses. On both CT scans and MRIs, proteinaceous debris in the trigone or occipital horn of the lateral ventricle and intense enhancement of the ependyma are seen.
  • Hydrocephalus: Ventriculomegaly can occur in the course of meningitis and is usually mild to moderate in severity (see Image 14). Obstructive hydrocephalus can occur with chronic inflammatory changes in the subarachnoid space or ventricular obstruction.

Degree of Confidence

With MRI especially, nonenhanced studies performed in patients with uncomplicated acute bacterial meningitis may demonstrate unremarkable findings; however, such results do not exclude acute meningitis.

False Positives/Negatives

Meningeal enhancement is nonspecific and may be caused not only by bacterial meningitis but also by neoplasm, hemorrhage, sarcoidosis, and other noninfectious inflammatory disorders.

ULTRASOUND

Section 7 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Findings

Bacterial meningitis is usually a clinical diagnosis. US is needed only to evaluate complications or a deterioration in the patient's clinical situation. Commercially available equipment is used with a 3- to 7.5-MHz transducer, depending on the size of the patient's head. Transducers of 5-7.5 MHz are used for newborns, whereas transducers of 3-5 MHz are used for older infants.

In newborns and older infants, complications of meningitis that are depicted on cranial CT scans and MRIs can also be demonstrated on cranial sonograms obtained with a transfontanel approach.

Important US findings in infants with bacterial meningitis have been described. These findings include echogenic sulci, ventriculomegaly and obstructive hydrocephalus, ventriculitis, prominent leptomeninges, subdural effusions, empyema, parenchymal echogenicity, and abscess formation. US can help to identify these complications, but the findings are usually not specific.

• Echogenic sulci that appear as a result of the accumulation of inflammatory debris are the most common and transient US finding in meningitis; these resolve gradually as the exudate is cleared.
• Mild to moderate ventriculomegaly, which is usually reversible, can occur in the course of meningitis. Exudates may produce CSF loculations and pathway obstruction, resulting in a communicating hydrocephalus, whereas obstructive hydrocephalus may occur with ventricular obstruction or chronic inflammatory changes in the subarachnoid space. Intraventricular septa formation may result in ventricular compartmentalization. Progressive ventriculomegaly can be excluded with the use of serial sonograms.
• Ventriculitis, which is seen in 65-90% of patients, is suggested by the US findings of hydrocephalus, which include a thickened, hyperechoic, irregular ependymal surface and echogenic debris and fibrous septa formation within the enlarged ventricles. The septa occur over the 2 weeks following bacterial meningitis; US is best for identifying septa, compared with CT scanning or MRI.
• Subdural effusion is a common US finding in infants with H influenzae meningitis. Subdural empyemas are uncommon findings and result when the effusions become infected.
• Areas of abnormal parenchymal echogenicity are a significant finding. The lesions represent cerebritis, infarction, encephalomalacia, or, rarely, abscess formation. Abscesses appear as homogeneous echogenic masses with a hypoechoic center that is surrounded by a thin hyperechoic rim.
• Doppler US can easily demonstrate the major intracranial vessels via the anterior transfontanel approach; however, in older children, these vessels can be demonstrated via the transtemporal approach. The cerebral blood flow can be evaluated qualitatively. Serial transcranial Doppler examinations performed to assess for disease-related arterial narrowing have been described. An association between an unfavorable course of the disease and increased cerebral blood flow velocity in intracranial arteries has been suggested; this probably indicates vasospasm. Transcranial Doppler US can potentially be used to identify high-risk patients who can benefit from adjuvant therapeutic interventions.

Degree of Confidence

US is a heavily operator-dependent technique. Experience is needed to demonstrate the meningeal and parenchymal findings of bacterial meningitis.

False Positives/Negatives

On US, inflammatory debris in the CSF creates low-level intraventricular echoes in acute ventriculitis. This appearance may imitate that which is seen in the breakdown of intraventricular hematomas; however, these 2 clinical settings can usually be distinguished because ventriculitis has other signs of inflammation.

NUCLEAR MEDICINE

Section 8 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Findings

Although CT scanning and MRI are the most common imaging modalities used to evaluate patients with a possible abscess, distinguishing brain abscesses with these 2 modalities is occasionally difficult. Technetium-99 (^99mTc) hexamethylpropyleneamine oxime, which is a radionuclide imaging label for leukocytes, and radiolabeled polyclonal immunoglobulin antibodies may be helpful in select patients. ^99mTc hexamethylpropyleneamine oxime may also be used in the evaluation of the cerebral blood flow velocity and perfusion in bacterial meningitis. In addition, radionuclide cisternography may depict CSF leaks, which may be the source in cases of recurrent meningitis.

ANGIOGRAPHY

Section 9 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Findings

Arterial angiography may demonstrate arterial spasm or may show focal areas of inflammation that have manifested by hypervascularity.

If magnetic resonance venography is not available, a reliable and cost-effective method for detecting venous sinus thrombosis is intravenous digital-subtraction angiography.

INTERVENTION

Section 10 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Medical/Legal Pitfalls

• The failure to diagnose bacterial meningitis can result in mortality or serious, permanent neurologic deficit.

• Identifying cerebral complications early is important. Some complications, such as symptomatic hydrocephalus, subdural empyema, and cerebral abscess, require prompt neurosurgical intervention.

• Inappropriate lumbar puncture may occur. This procedure must not be performed in patients who may have possible increased intracranial pressure. Normal CT scan findings may not be sufficient evidence of normal intracranial pressure in patients with bacterial meningitis.

Special Concerns

• The clinical presentation of bacterial meningitis varies with the age of the patient.
• If a patient has been taking antibiotics for another infection, the symptoms of meningitis can take longer to develop, or they may be less intense.

MULTIMEDIA

Section 11 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Media file 1:  Chronic mastoiditis and epidural empyema in a patient with bacterial meningitis. This axial computed tomography scan shows sclerosis of the temporal bone (chronic mastoiditis), an adjacent epidural empyema with marked dural enhancement (arrow), and the absence of left mastoid air.
	View Full Size Image
Media type:  CT

Media file 2:  Frontal sinusitis, empyema, and abscess formation in a patient with bacterial meningitis (same patient as in Images 3-4). This contrast-enhanced, axial T1-weighted magnetic resonance image shows a right frontal parenchymal low intensity (edema), leptomeningitis (arrowheads), and a lentiform-shaped subdural empyema (arrows).
	View Full Size Image
Media type:  MRI

Media file 3:  Frontal sinusitis, empyema, and abscess formation in a patient with bacterial meningitis (same patient as in Images 2 and 4). This T2-weighted axial magnetic resonance image shows frontal sinusitis, a bone defect (arrow) with adjacent cortical edema (arrowhead), and right occipitoparietal subdural fluid collection (empyema).
	View Full Size Image
Media type:  MRI

Media file 4:  Frontal sinusitis, empyema, and abscess formation in a patient with bacterial meningitis (same patient as in Images 2-3). This T2-weighted axial magnetic resonance image shows a developing abscess formation with mass effect and bilateral subdural fluid collections (empyema).
	View Full Size Image
Media type:  MRI

Media file 5:  Cerebritis and developing abscess formation in a patient with bacterial meningitis (same patient as in Images 6-7). This contrast-enhanced, axial computed tomography scan was obtained 1 month after surgery and shows a small, ring-enhanced, hypoattenuating mass (recurrence of abscess) in the left basal ganglia and a left lentiform-shaped subdural fluid collection with enhanced meninges (arrowhead).
	View Full Size Image
Media type:  CT

Media file 6:  Cerebritis and developing abscess formation in a patient with bacterial meningitis (same patient as in Images 5 and 7). This contrast-enhanced axial computed tomography scan shows leptomeningitis and parenchymal enhancement (cerebritis) with a low-attenuating area (edema) in the left basal ganglia.
	View Full Size Image
Media type:  CT

Media file 7:  Cerebritis and developing abscess formation in a patient with bacterial meningitis (same patient as in Images 5-6). This contrast-enhanced axial computed tomography scan shows a ring-enhancing, lobulated, hypoattenuating mass (abscess) in the left basal ganglia.
	View Full Size Image
Media type:  CT

Media file 8:  Subdural empyema and arterial infarct in a patient with bacterial meningitis. This contrast-enhanced axial computed tomography scan shows left-sided parenchymal hypoattenuation in the middle cerebral artery territory, with marked herniation and a prominent subdural empyema.
	View Full Size Image
Media type:  CT

Media file 9:  Watershed and lacunar infarcts in a patient with bacterial meningitis. This axial computed tomography scan shows a left frontoparietal watershed infarct, a right basal ganglia lacunar infarct, and a bilateral subdural effusion.
	View Full Size Image
Media type:  CT

Media file 10:  Subdural empyema and diffuse cerebral edema in a patient with bacterial meningitis (same patient as in Image 11). This axial computed tomography scan shows bilateral subdural effusion (empyema) and parenchymal low-attenuating areas.
	View Full Size Image
Media type:  CT

Media file 11:  Subdural empyema and diffuse cerebral edema in a patient with bacterial meningitis (same patient as in Image 10). This contrast-enhanced computed tomography scan was obtained 1 week after the one in Image 10 and shows diffuse cerebral edema and lacunar infarcts in the thalamus.
	View Full Size Image
Media type:  CT

Media file 12:  Abscess in a patient with bacterial meningitis. This contrast-enhanced computed tomography scan shows a ring-enhancing, hypoattenuating mass (abscess) with peripheral edema and mass effect.
	View Full Size Image
Media type:  CT

Media file 13:  Acute bacterial meningitis (same patient as in Images 14-15). This axial nonenhanced computed tomography scan shows mild ventriculomegaly and sulcal effacement.
	View Full Size Image
Media type:  CT

Media file 14:  Acute bacterial meningitis (same patient as in Images 13 and 15). This axial T2-weighted magnetic resonance image shows only mild ventriculomegaly.
	View Full Size Image
Media type:  MRI

Media file 15:  Acute bacterial meningitis (same patient as in Images 13-14). This contrast-enhanced, axial T1-weighted magnetic resonance image shows leptomeningeal enhancement (arrows).
	View Full Size Image
Media type:  MRI

Media file 16:  Pachymeningitis in a patient with bacterial meningitis. This contrast-enhanced, axial T1-weighted magnetic resonance image shows diffuse dural enhancement.
	View Full Size Image
Media type:  MRI

Media file 17:  Pachymeningitis and cerebritis in a patient with bacterial meningitis (same patient as in Image 18). This contrast-enhanced, T1-weighted axial magnetic resonance image shows left-sided dural enhancement (pachymeningitis) and focal pial enhancement.
	View Full Size Image
Media type:  MRI

Media file 18:  Pachymeningitis and cerebritis in a patient with bacterial meningitis (same patient as in Image 17). This T2-weighted axial magnetic resonance image shows parenchymal focal edema (cerebritis).
	View Full Size Image
Media type:  MRI

Media file 19:  Subdural empyema with strand in a patient with bacterial meningitis. This contrast-enhanced, axial computed tomography scan shows a bilateral subdural effusion with cortical surface enhancement (empyema). Note that the attenuation of the effusion is higher than that of the cerebrospinal fluid.
	View Full Size Image
Media type:  CT

Media file 20:  Ventriculitis in a patient with bacterial meningitis. This contrast-enhanced computed tomography scan shows ependymal enhancement.
	View Full Size Image
Media type:  CT

Media file 21:  Lacunar infarct in a patient with bacterial meningitis. This axial computed tomography scan shows the distribution of the perforating vessels in the brainstem, basal ganglia, and white matter.
	View Full Size Image
Media type:  CT

Media file 22:  Bilateral subdural empyema in a patient with bacterial meningitis. This computed tomography scan demonstrates the important diagnostic features of meningitis: prominent enhancement of the margin and increased attenuation of the empyema.
	View Full Size Image
Media type:  CT

Media file 23:  Abscess formation in a patient with bacterial meningitis. This contrast-enhanced, T1-weighted, axial magnetic resonance image shows an abscess formation in the right frontal lobe (arrows) and a right parasagittal subdural empyema (arrowhead).
	View Full Size Image
Media type:  MRI

Media file 24:  Pachymeningitis in a patient with bacterial meningitis. This contrast-enhanced, T1-weighted, coronal magnetic resonance image also shows subdural empyemas on the left side.
	View Full Size Image
Media type:  MRI

REFERENCES

Section 12 of 12

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

1. Moses S. Meningitis: acute bacterial meningitis. Revised 5/28/2007. Available at http://www.fpnotebook.com/NEU149.htm. Accessed May 29, 2007.
2. Kioumehr F, Dadsetan MR, Feldman N, et al. Postcontrast MRI of cranial meninges: leptomeningitis versus pachymeningitis. J Comput Assist Tomogr. Sep-Oct 1995;19(5):713-20. [Medline].
3. Runge VM, Wells JW, Williams NM, et al. Detectability of early brain meningitis with magnetic resonance imaging. Invest Radiol. Aug 1995;30(8):484-95. [Medline].
4. Ashwal S. Neurologic evaluation of the patient with acute bacterial meningitis. Neurol Clin. Aug 1995;13(3):549-77. [Medline].
5. Auburtin M, Wolff M, Charpentier J, et al. Detrimental role of delayed antibiotic administration and penicillin-nonsusceptible strains in adult intensive care unit patients with pneumococcal meningitis: the PNEUMOREA prospective multicenter study. Crit Care Med. Nov 2006;34(11):2758-65. [Medline].
6. Becker LE. Infections of the developing brain. AJNR Am J Neuroradiol. Mar-Apr 1992;13(2):537-49. [Medline].
7. Brouwer MC, van de Beek D, Heckenberg SG, Spanjaard L, de Gans J. Hyponatraemia in adults with community-acquired bacterial meningitis. QJM. Jan 2007;100(1):37-40. [Medline].
8. Chang YC, Huang CC, Wang ST, Chio CC. Risk factor of complications requiring neurosurgical intervention in infants with bacterial meningitis. Pediatr Neurol. Sep 1997;17(2):144-9. [Medline].
9. Chen CY, Huang CC, Chang YC, et al. Subdural empyema in 10 infants: US characteristics and clinical correlates. Radiology. Jun 1998;207(3):609-17. [Medline].
10. Dichgans M, Jäger L, Mayer T, Schorn K, Pfister HW. Bacterial meningitis in adults: demonstration of inner ear involvement using high-resolution MRI. Neurology. Mar 23 1999;52(5):1003-9. [Medline].
11. Djeric DR, Schachern PA, Paparella MM, et al. Otitis media (silent): a potential cause of childhood meningitis. Laryngoscope. Dec 1994;104(12):1453-60. [Medline].
12. Fitz CR. Inflammatory diseases of the brain in childhood. AJNR Am J Neuroradiol. Mar-Apr 1992;13(2):551-67. [Medline].
13. Geyer JD, Nabors LB, Harrell LE, Gomez CR. Magnetic resonance cisternography in the diagnosis of delayed iatrogenic cerebrospinal fistula: a case report. J Neuroimaging. Oct 1997;7(4):244-7. [Medline].
14. Gjini AB, Stuart JM, Cartwright K, et al. Quality of in-hospital care for adults with acute bacterial meningitis: a national retrospective survey. QJM. Nov 2006;99(11):761-9.